Feline cholangitis and chronic pancreatitis (Proceedings)
Liver disease is common in the cat and the finding of icterus is a frequently a clinical clue that the cause is primary liver disease. The types of liver disease as well as differences in laboratory tests for the cat are very different from disorders observed in the dog.
A sick cat may become icteric (jaundice) without having primary liver disease. This is because of the complexities of bilirubin metabolism combined with cat's weak ability to conjugate compounds. It is this complex pathway that can result in icterus without evidence of significant structural liver disease. Cats with clinically icteric (bilirubin > 3.0 mg/dl) most often have primary hepatobiliary disease when hemolytic disease is ruled out. Cats having biochemical icterus (bilirubin < 3.0 mg/dl) do not always have primary hepatobiliary disease and many have other primary non-hepatic disorders with the liver being secondarily affected.A study evaluating the utility of liver biochemistries in the diagnosis of feline liver disease found the best predictive tests for primary liver disease includes ALP, GGT, total bilirubin and bile acids. The ALT and AST are quite variable and elevations don't always predict primary inflammatory liver disease or hepatic lipidosis, both of which cause more cholestatic (increases in ALP, GGT) than hepatocellular (increases in ALT, AST) damage. ALP is also unique in cats in that the half-life of the enzyme is short (6 hours) and the feline liver is reported to contain only one-third the concentrations found in dogs. ALP is also not induced by corticosteroids nor do they cause a steroid hepatopathy. Gamma-glutamyl transpeptidase (GGT) is a similar enzyme to ALP that increases with cholestasis and is more sensitive for feline inflammatory bile duct disease than ALP. Presumably this is because GGT is found in higher concentrations in the bile ducts than the hepatocyte where ALP predominates. Cats with cholangitis usually have higher elevations in GGT than ALP.
The incidence of liver disease in the cat is unknown but at Colorado State University several large categories were observed in reviewing 175 liver biopsies and include: Lipidosis (both idiopathic and secondary, 26%), Cholangitis (25%), Neoplasia (20%) and Reactive hepatopathies (16%).
Hepatic lipidosis can occur as either a primary idiopathic disease syndrome or secondary to a number of other primary disease conditions. Lipid accumulation in the liver is simply the result of nutritional, metabolic or toxic insults to the liver and the degree of lipid accumulation can be quite variable and the process is reversible. For example, a common secondary disease associated with significant hepatic triglyceride accumulation is diabetes mellitus. Hepatic lipid accumulation can also result secondary to any number of other disease syndromes associated with anorexia and weight loss such as pancreatitis, inflammatory bowel disease or other major organ dysfunction. These secondary conditions generally have less severe lipidosis than idiopathic hepatic lipidosis in which there is no identifiable etiologic factor.
In the idiopathic form cats will present with an acute history of rapid weight loss (up to 40-60% body weight over 1-2 weeks), depression and icterus. The weight loss is significant with loss of muscle mass while abdominal and inguinal fat stores are often spared. These cats generally have a total aversion to any type of food. The diagnosis of idiopathic hepatic lipidosis is supported by the clinical history and laboratory findings. Icterus and marked elevations in ALP are consistent findings. GGT concentrations are normal or only moderately increased in these cats. Icterus with a very high ALP and normal GGT should be a clue to probable idiopathic lipidosis given with appropriate clinical features.
A definitive diagnosis requires a liver biopsy or hepatic cytology. A fine needle aspirate of the liver with cytological evidence of many vacuolated hepatocytes helps support a diagnosis. Be aware that cytological diagnosis does not always correlate with histology. A hepatic tissue biopsy confirms the diagnosis of lipidosis but not the cause.
The therapy for idiopathic hepatic lipidosis requires aggressive management. Initial therapy requires re-hydration with balanced electrolyte solutions. Administration of high glucose containing solutions and lactate-containing fluids should be avoided.